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ARP101 inhibits α-MSH-stimulated melanogenesis by regulation of autophagy in melanocytes.

FEBS letters (2013-11-06)
Eun Sung Kim, Yoon Kyung Jo, So Jung Park, Huikyoung Chang, Ji Hyun Shin, Eun Sun Choi, Jun Bum Kim, Su Hyeon Seok, Jae-Sung Kim, Jeong Su Oh, Myoung-Hwan Kim, Eunjoo H Lee, Dong-Hyung Cho
ZUSAMMENFASSUNG

Autophagy is a cooperative process between autophagosomes and lysosomes that degrades cellular organelles. Although autophagy regulates the turnover of cellular components, its role in melanogenesis is not clearly established. Previously, we reported that ARP101 induces autophagy in various cancer cells. Here, we show that ARP101 inhibits melanogenesis by regulation of autophagy. ARP101 inhibited α-MSH-stimulated melanin synthesis and suppressed the expression of tyrosinase and TRP1 in immortalized mouse melanocytes. ARP101 also induced autophagy in melanocytes. Knockdown of ATG5 reduced both anti-melanogenic activity and autophagy mediated by ARP101 in α-MSH treated melanocytes. Electron microscopy analysis further revealed that autophagosomes engulf melanin or melanosome in α-MSH and ARP101-treated cells. Collectively, our results suggest that ARP101 inhibits α-MSH-stimulated melanogenesis through the activation of autophagy in melanocytes.

MATERIALIEN
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Produktbeschreibung

Sigma-Aldrich
Tyrosinase aus Ständerpilz, lyophilized powder, ≥1000 unit/mg solid
Sigma-Aldrich
α-Melanozyten-stimulierendes Hormon, ≥97% (HPLC)
Sigma-Aldrich
Anti-Aktin-Antikörper, Klon C4, ascites fluid, clone C4, Chemicon®